Morning, everybody. My name is Chelsea Kimura. I am an Inupiaq descendant and I'm a social worker by training and I now serve as a training and technical specialist for the Opioid Response Network. For those of you who may not be familiar with the Opioid Response Network, we are grant funded by SAMHSA to provide free training and technical assistance to tribal opioid response grantees and other native communities across the country. Today, we're gonna be sharing a session about brain science and the impact of opioids on the brain. And before I introduce our presenter for today's session, I would really like to open our session in a good way today by sharing a land acknowledgement. So our work... We're not muted. Sorry. No worries, you're good. So our land acknowledgement, our work intends to reach the addiction workforce in the Northwest TOR region. This includes Alaska, Idaho, Oregon, and Washington. This region rests on the ancestral homelands of the indigenous peoples who have lived on these lands since time immemorial. Please join us in support of efforts to affirm tribal sovereignty and in displaying respect and gratitude for our indigenous neighbors. We respectfully acknowledge and honor all indigenous communities, past, present, and future. And with that, it's my honor to introduce our presenter for today's session, Stephanie Stillwell. Stephanie is a registered nurse with a diverse background in the healthcare industry, and she has a background in addiction treatment and healthcare consulting. Her passion is promoting community health and wellness and disease prevention. Stephanie works creatively to bridge the gap between the healthcare system, individuals, and the community. She's facilitated multiple local and statewide coalitions throughout the state of Alaska. Stephanie is an Anishinaabe woman from Lac La Croix First Nation in Ontario, Canada. And I will go ahead and pass this over to Stephanie to start us off today. Thank you, Stephanie. Hi, everybody. It's nice to be here with you today. I am going to, as Chelsea mentioned today, this is the first of multiple sessions that we'll have together. And we're gonna start out by diving into the brain science of addiction and the impact of opioids on the brain. So let me make sure my, here we go. And just to let everybody know, I don't have any relevant disclosures or financial gain from anything that I'm presenting to you today. And I'm not going to dive into the ORN as Chelsea already gave you all that information. But like I said, today is the first of four sessions on opioids and medication for opioid use disorder treatment. So over the next month or so, we'll be diving into different aspects of opioid use disorder, including the brain science, which is today. Then we'll talk more about the risk and prevention factors, treatment, including medication for addiction treatment, some harm reduction. And then the sessions that we'll end on are going to be a deeper dive into stigma and trauma-informed practices and really how we can kind of incorporate all of this into the work that we're doing. So again, today, we're gonna focus on understanding kind of a little bit more about what substance use disorder really is and the impact that substance use disorder has on the brain and understanding how opioids really work within our body. So this is gonna help lay the foundation to better understand how treatment, specifically medication for opioid use disorder work and why they're considered really our gold standard practice in treatment today. So what is substance use disorder? So substance use disorders are diagnosed medically using something called the DSM-5, which is a diagnostic manual that is widely used by healthcare providers and physicians to identify different mental health conditions. What's different about this method of diagnosing is it doesn't involve lab tests and blood draws and urine screenings to tell us the results. Really, this is based more on observable behaviors. So the DSM-5 categorizes substance use disorder into kind of like four different key domains, which encompass a total of 11 different criteria. So these criteria cover issues such as impaired control. So this is using more of a substance or more often than intended. If somebody is wanting to cut down on or stop using, but they're not able to. Folks who might be spending a great deal of time obtaining, using, or recovering from the effects of a substance use or experiencing cravings or kind of more of a pressing desire to use a substance. And then we have social problems, neglecting responsibilities, relationships, giving up on activities that they once cared about because of their substance use. An inability to complete tasks at home, work, school. Then we have risky use, which is kind of using in risky situations or settings. Continued use despite knowing that this is causing problems and then we have the like physical dependence aspect of it. So these are the only two physical aspects of the diagnostic criteria. And that is the physical dependence of needing to have more substance to get the same effect, which is what we call tolerance and having a withdrawal symptom when that substance is not used. So again, what's really important to understand is that this disease, about this disease is that the criteria to diagnose is exclusively based on those behaviors rather than those lab-based assessments. So because of this, because of how they're diagnosed, it's really important to realize that it can be really inappropriate if a healthcare provider says, they are going to dismiss a person from treatment solely based on kind of the signs and symptoms of the disease itself. So things that are often thought of as like behavioral problems, like showing up, not showing up to appointments or having trouble with certain follow-through for parts of their treatment. That's actually really something that we need to look at as a symptom of the disease process rather than like a source of frustration or dismissal from treatment. So additionally, there's different levels of severity when it comes to substance use disorders. So if you have a presence of two to three of these symptoms, you're considered to have a mild SUD. Four to five symptoms are moderate. And then if you have more than six symptoms present, then that's considered more of a severe substance use disorder. And I also want to let you folks know, if you have questions along the way, please reach out. We'll have some time at the end of the discussion to go over some questions as well, but just feel free to come online and ask. Also in regards to substance use disorders, it's important to recognize that we can view this kind of on the spectrum. As we talked about, we have different levels of severity of substance use disorders. It's also important to note that there's kind of a different spectrum of substance use. We have, of course, all the way from the beginning, we have non-use. This is completely abstinent from all substances all the way to substance use disorder. And then there's something that we sometimes see as beneficial use, which it's important to note that even though things might be listed as beneficial, there's always a risk of developing a substance use disorder at any point. So it's really important to recognize that. But one of the examples of a beneficial use of a substance is that in most, a lot of our indigenous communities, we have tobacco as one of our sacred medicines that we use and it's used in spiritual and cultural ceremonies. And so kind of one of the concepts behind that is kind of honoring that sacred use of the tobacco rather than, as opposed to having a nicotine use disorder. And now we're going to kind of dive into a little bit more of the brain science of substance use disorders, generally speaking, and then we'll kind of get more specific about the opioids in particular. So the brain, of course, is a really complex organ and the science of the brain is really important complex organ and the science behind how our brain works, just generally speaking, is really detailed, intricate, and I can't, I'm not a neuroscientist, so I can't tell you everything, but what I do want to do today is to be able to give you a little bit of information to walk away and understand a bit more about kind of like what is happening in our brains on day to day, especially when substances are included in our body. So I have a video that we're going to watch for about five-ish minutes that does a really good job of kind of explaining this process. And then we're going to kind of break down a little bit from the video. So I'm going to go ahead and start playing the video. Let me know if you're having any issues hearing. Let's see if my technology is working. You need three things to survive. You need food, you need water, you need dopamine. Now, some of the people who get a little antsy say we also need oxygen. Yes, well, we also need skin, but I'm not going to really talk about that today. We're going to talk about the three things we absolutely need to survive as a human in today's world, and that is food, water, and dopamine. We need dopamine because it's the chemical responsible for motivation. It's this thing that's responsible for us going and making a friend, having a mother have a bond with a baby. It's the thing that motivates us when we do good to do better. When somebody pats you on the back and says, good job, and you go to do something more significant, that's because your dopamine has gotten pinged, and it's just something pushing you, this invisible chemical that's pushing you along the path. On a normal day, we even know how much dopamine we're supposed to have. On Monday morning when I wake up and I have to get up and I go to work, I live in the range of about 50 nanograms per deciliter of dopamine. That sits in the central part of my brain, and that's required for me to get out of bed and go get that first cup of coffee. Now, what about the worst day, the really bad day, the day you call your office and you fake vomit in the phone and you decide not to go in? You're like, I just can't make it. That's about 40 nanograms per deciliter, so not much lower, but low enough to where you just want to sit around in your pajamas all day and do nothing. What about the best day ever? You know, the day where all at once you win the lottery, you have 2% body fat, and you're living on the beach? All of those things happen at the exact same time? We even know that one. That's 100 nanograms per deciliter. Our brain is meant to go all the way to there. It's not really meant to go above. And we can look at things like your favorite food, which is like 94 nanograms per deciliter, and sex, 92 nanograms per deciliter. Bummer, right? Couldn't have predicted that. Maybe they need to redo that research. But at the same time, we know that we're supposed to live within this relative normal state between 40 on a horrible day and 100 on our best day. So what happens when we add a chemical into the brain like methamphetamine? This chemical is really important because it pushes us way past that 100 nanograms per deciliter. In fact, it actually pushes up to 1,100 nanograms per deciliter, more than 10 times the amount of dopamine that our brain should be making. And then if we look at things like marijuana or alcohol or heroin, these are things that push it up into the high hundreds. This is not what we're supposed to be doing. As we look at this, we have the normal that we're supposed to be. We have this large jump for something like methamphetamine. And then we have these other drugs that drive that dopamine up. And when that happens, it starts to take over that part of the brain. And no longer does going to your child's birthday make you happy. It's not happening. The things that normally make us feel happy start to pale in comparison. This is because the brain is built to survive. In fact, we know that this is a survival issue for the brain, mainly because dopamine is what drives us to procreate, to get food, to get water, like we talked about. And we know so much about addiction and all of these things that are going on in that part of the brain that we actually know the parts of the brain responsible for this motivation in this dopamine release. It's places like the anterior cingulate gyrus, the lateral bed nuclei of the amygdala, the nucleus accumbens, the ventral tegmental area, the periaqueductal gray. We know this. And by the end of all of these videos on this site, you're going to know exactly what each of those parts do. But for now, you should understand that this area of the brain called the limbic system, which includes, but it's not limited to, the ventral tegmental area and the nucleus accumbens are responsible for reward. And the fact that we can look on an MRI and see these parts of the brain working and we can see them working in a patient who is not on any drugs and those that have been on illicit substances for a long time and see major differences in how these structures work is really important because it allows us to start to understand things like behavior. We can see that all of the focus is on the dopamine part of the brain. Remember that nucleus accumbens and ventral tegmental area that we talked about. In that part of the brain, when you've been taking things like methamphetamine for a long time, every time that you take the methamphetamine it goes from 1,100, then the next time maybe it's 900, then 600, then 500, then 200, then 100. Then you're required to take that drug even to get you up to that normal level of 50 nanograms per deciliter. Let's say we found this person, we get them into treatment and we remove that drug. Now we have people whose dopamine goes all the way down to as low as 10 nanograms per deciliter. And on their best day ever, it's only 20 nanograms per deciliter. These are numbers that matter and we're gonna keep hammering on these because when you have 10 nanograms per deciliter, you can't get out of bed. You can't get up to put your clothes on and go to a job interview or to even take care of yourself or your family. When we lack dopamine, the body craves it. And when you crave dopamine, you get into survival mode. And that leads to primal action. And that primal action is a lot of times the behavior that we see. How can they take grandma's jewelry? How can they steal a credit card? How can they pawn something that they own? Their brain is telling them that they are not going to survive if they don't get dopamine. And the thing that gives them the dopamine that they need as far as they know, is that drug of choice. Behavior is so much about how three things to survive. Three things to survive. Okay. So sorry about the video there. We'll be coming back to the video kind of throughout the series a little bit. And I'm definitely going to come back and talk about things that we're watching in that video. But this really, you know, this is a chart that really kind of describes the dopamine levels that he was referring to in that clip with the different substances. So as you can see, with the different types of substances has different impacts of the dopamine in our brains. And so on to the next here. And when it comes to the dopamine receptors in our brains, obviously we know that repeated drug use does change our brains. So repeated use of cocaine and other drugs reduces the levels of dopamine in our brain. And so here is just kind of some images that describe the actual dopamine interference that is caused with drug use over time. But one of the good things about our brain is that our brains actually are one of the organs that can recover. So our brain function can also recover. And so this is just another image that really does show. So this is in a normal control. So somebody who does not use any type of substances or anything and what the dopamine might look like, the transporters look like in the brain and how active they are. Of course, the more red they are, the more they're used. And then this is somebody who had been using methamphetamine and then a repeated scan after one month. So you can see this is definitely a decrease in activity in the dopamine transporters here. But the same person 14 months later, they have regained almost back all of their function. So of course, over the course of that time, they had to allow their bodies and their brains to recover to get back to their normal baseline levels of dopamine in their brains. So now we're going to kind of dive a little bit more into opioids and fentanyl, specifically in opioid use disorder. So I just wanted to start by sharing this graph. So of course, as you can see, over the number of 20 years or so, we've experienced a steady kind of increase in the number of overdose deaths. And this is nationally, so in the United States over the course of time. And there's kind of been a few different waves of overdoses in the last 20 years. And so we have the first wave started in the early 2000s, and then middle 2000s around 2013, and then a major increase in the later part. And so if you're looking at the different types of substances that are involved in these overdoses, it kind of moves across from heroin as one of the bigger overdose substances to synthetic opioids, and this is primarily fentanyl. And of course, there's also prescription opioids in there as well. So heroin, prescription opioids, and then now what we are seeing is that fentanyl, the synthetic opioids. And, you know, in our next session, we're going to talk a lot more about like the risk factors and who and why people kind of develop opioid and substance use disorders. And we're really going to touch on a lot more of like why Indigenous communities and factors that Indigenous communities experience that create kind of a more disproportionate impact from substance and opioid use disorders. But in the United States, Indigenous communities significantly face more impacts from opioid use disorder due to a lot of different things like, you know, historical trauma, socioeconomic factors, maybe there's more limited access to healthcare, higher rates of trauma, and even certain prescribing practices in different settings. So there's a lot of number of reasons. But if we're just looking at this, this map or this graph here, these are just overdose deaths involving opioids in the American Indian Alaska Native population. So that's quite significant. And so it's really important to talk about why and to talk about and educate tribal communities about opioids and the risks and how we can really help to make a change, a positive change in working in these communities and decreasing the amount of opioids in our communities. So now we're going to kind of dive into a little bit more about the opioids in particular and the terminology around them. So I'm sure some of you have heard them referred to as opiates and opioids. So can I talk a little bit about the difference between those? So we have opiates, which are naturally occurring compounds that are actually present in nature. They come from the seed pods of, well, it's opium, and those come from the seed pod of something called a papiver somniferum plant, which also is called the poppy plant. So some of the examples that are opiates that are derived from the opium of poppy plants are things like morphine and codeine. And then we have the synthetic opioids. These ones are the ones that are kind of chemically synthesized in a lab that mimic the effects and impact of natural opiates. So these are manufactured in labs. The synthesis of these synthetic opioids involve creating the chemical compounds that look very similar to those of the natural opiates. Opioids are then broken down into different semi-synthetics and synthetics. So semi-synthetics are things such as the vicodin, the hydrocodone, and the hydromorphone. And then we have the full synthetic lab-made opioids, which are fentanyl, methadone, and even buprenorphine. And heroin is also a semi-synthetic opioid, and that is made from the morphine that was chemically processed. So heroin also fits into the semi-synthetics here. All right, and another video. This one's a lot shorter, and it's really just to kind of help share the neuroscience of opioids, so what is really happening in our brain specifically when we introduce opioids to our body. So here we go, another video. Sorry about that. There we go. That was not part of the... Neither is this. I don't know why there's ads. There's never ads. My name is Ryan Kurzeski. There we go. I'm a commercial producer here at Reliable Agency. This is not part of my presentation, so sorry. You can buy your insurance from anybody. Why should you buy it from anybody? I'm a commercial producer here at Reliable Agency. This is not part of my presentation, so sorry. You can buy your insurance from anybody. Why should you buy it from anybody? Why should you buy it from me? Why should you buy it from Reliable? It's because we genuinely care about each other. All of that stuff spills over to caring about your clients. When they are at their most vulnerable, they have to call you and rely on you to make sure that they're taken care of. Okay. This is Susan. Susan loves to bike. While out for a ride, she falls and breaks her arm. Special cells called neurons send a signal through the spinal cord to the brain, which interprets the signal as pain. Susan understands the pain means she needs to go to the hospital, and her body is equipped for survival, helping her not to panic so she can seek help. Many of her neurons are covered in proteins called opioid receptors. These receptors act like a brake to slow down the neuron's ability to send pain signals. When injured, her body releases natural painkillers called endorphins. Like a key in a lock, endorphins activate opioid receptors, slowing down the pain signal and preventing a panic. Susan gets treated for the broken bone. But three months later, her arm still hurts. And now that pain is making her feel depressed and anxious. So her doctor prescribes an opioid painkiller. There are many different opioids, but they all share a chemical similarity to our own endorphins. This allows them to bind to the same opioid receptors and stop pain signals. But that's not all they do. Deep inside Susan's brain is a region called the ventral tegmental area, or VTA for short. The VTA is full of neurons that produce a chemical called dopamine. When something good happens, dopamine is released, giving Susan a feeling of pleasure. This helps teach her brain to keep seeking out good things. To keep dopamine neurons in check, inhibitory neurons keep the brakes on until something good comes along. Just like the pain neuron, these neurons are covered in opioid receptors. When Susan takes the painkiller prescribed by her doctor, the opioid receptors turn off the inhibitory neurons and release the brake on the dopamine neurons. The rush of dopamine temporarily eliminates Susan's depression and anxiety. And she feels relief, calmness, and even euphoria. As Susan continues to take the painkillers, her brain responds by trying to regain its balance. Her inhibitory neurons work extra hard even when the opioid receptors are activated. And it becomes harder and harder for her dopamine neurons to release dopamine. Susan finds that she needs to increase her dose of painkillers in order to feel comfortable. This is called tolerance. Eventually, Susan's pills run out. Inhibitory neurons that had been working overtime are let loose, clamping down on those dopamine neurons and shutting them off almost completely. Now, not only is Susan in pain, but the depression and anxiety come back. On top of that, Susan feels ravaged by an inescapable physical sickness far worse than any flu. Susan's body is going through withdrawal. Most people who take opioids for a long time tend to experience some withdrawal, but they can still stop taking the pills and return to normal. But for people like Susan, it's not so easy. Her genetics and the environment she grew up in put her at a higher risk for addiction. Her withdrawal symptoms aren't just unpleasant, they're unbearable. Susan thinks the only way to feel normal is to find more opioids. And this is how the cycle of opioid addiction emerges, driven by a brain trying to regain its balance. But there is hope for Susan. Though the road to recovery can be challenging and there may be setbacks, treatments can retrain Susan's brain. With the help of medication and therapy, Susan finds pleasure in her life once again. So before I change to the next screen, just kind of want to take a moment to again think back to the video we watched just a few minutes ago, where we really talked about the three things we need to survive, the food, water, and dopamine. So again, this video also highlights how the role of dopamine is in play when it comes to opioids as well. And they did highlight a little bit about the risk factors and genetics and environment, and we're going to talk more about that in our next session. So this is a little bit more clear picture of the impact that how opioids affect our brain. So the natural endorphins, which actually endorphins is the word, the word is short for endogenous morphine, are these endogenous opioids that are produced within our own brain. That are produced within our own body. So these are the molecules that really help us naturally play, help us respond to pain and stress. They act as those neurotransmitters and neuromodulators. And so this is a natural, normal system that is already happening in our brain. And so again, these endorphins interact with the body's natural opioid receptors, which are here. And then they impact the dopamine reward system. So when, again, naturally when this is activated, again, it does trigger a dopamine release that contributes to us feeling a little bit better. And these are often released by things that bring us pleasure, like exercise, social interactions, and other positive experiences. However, now when we're looking at when we take an opioid and put an opioid in our body, it's really kicking off these, kicking out these natural endorphins that we have in our system and replacing them with these kind of more intense opioids that bind into that same receptor. So when opioids are introduced into our body, whether it's through prescription medications or illicit drugs, they mimic the same action of the natural endorphins by binding to those same receptor sites. And then this, just to highlight again, the DSM, the diagnostic material for opioid use disorder is literally the same thing as substance use disorder, except we're looking at specifically opioids. So if opioids are taken in larger amounts, again, we still have the same 11 criteria with the two that are actually just the physical pieces of it, which is the tolerance and the withdrawal. But otherwise, we have the same four major categories and the 11 criteria altogether. And again, same thing, we can have opioid use disorder severities from mild, moderate to severe. And of course, when we are talking about opioids, we have these different physical effects of opioids. So one physical effect of taking an opioid is, of course, pain control. And that is something that isn't necessarily a bad thing when it's prescribed properly under the correct dosage and monitoring by a provider. But there's always, again, that risk of developing a tolerance. Or developing an opioid use disorder, even when it's prescribed to you from that provider. But intoxication of an opioid looks like slower breathing. It decreases our respiratory system, so it decreases our breathing, our heart rate drops, our blood pressure lows, lessens, sorry. We become more sleepy, slowed, sometimes slurring our words. It creates our pinpoint pupils, and oftentimes you'll kind of see some people nodding, nodding off to sleep. And then again, beyond that is when we are reaching overdose, which is of course when most of the time our overdoses are caused by respiratory distress, so we'll stop breathing. And then when we talk about withdrawal symptoms of opioids, we're really looking at the fast, kind of the opposite, right? So someone is going to be breathing really fast, have a really increased heart rate, high blood pressure, they're going to be really anxious and irritable, can't sleep, their pupils are very dilated, a lot of pain in their bodies, runny nose, sometimes you'll see people tearing up, and of course the unpleasant effects of nausea, vomiting, and diarrhea. And then with those comes other things like dehydration and those uncomfortable situations. But as that video did share, there's definitely recovery from opioid use disorder. There's multiple different treatments for this disorder, and recovery from OUD is really a journey that has a lot of different paths that people can take to achieve recovery, all the way from medication for addiction treatment and behavioral therapy, to other holistic approaches like having support groups, there's wellbriety, there's a lot of different Indigenous recovery principles as well. And every path is extremely unique and offers the individual the tools to kind of break free from that grip of substance use disorder. But it's really important for a person who is working on their recovery to kind of find the path that really works to support them the most on their journey. But from a medical standpoint, the gold standard treatment for opioid use disorder is to use medication for opioid use disorder treatment. And especially if we can combine that with behavioral therapy as well. So one other really important piece to note about medication for opioid use disorder is this is the only one that's really unique to also reducing mortality related to opioid use disorder. As we kind of looked at the diagnostic criteria for opioid use disorder, we have to recognize that sometimes recurrence or what people might have called before relapse is part of the kind of the diagnosis. So when we are looking at trying to do the best to prevent mortality and overdoses, using a medication for our treatment is going to be the way to help reduce accidental overdose in that. So when we're looking at medications for opioid use disorder, we're really talking about most of the time three different medications, such as methadone, buprenorphine, and naltrexone. They each operate in our brain different ways to help folks kind of work through their addiction. And oftentimes MAT, medication for addiction treatment, you'll hear me call it MAT and MOUD, which is medications for opioid use disorder. But MAT works by oftentimes decreasing the craving that is associated with substance use disorder. So again, if we're thinking back to the three things that we all need to survive is food, water, and dopamine, you know, that dopamine is really what we're talking about when we're talking about craving. So we have a whole nother presentation that we'll get to when we, and we'll dive deeper into medications. But today I'm going to just kind of do a brief overview. But we have a couple of different types of medications here. So we have methadone, which we call a full agonist. And a buprenorphine is also an agonist, but it's only a partial agonist. What these do is they kind of act and they activate the same receptor sites as opioids, but just have like milder effects than if you were to take an opioid medication. And so what this does is it helps to both reduce the cravings associated with the opioid use disorder, as well as reducing the withdrawal symptoms. So methadone takes, it's kind of fills the entire opioid receptor, similarly to what an actual opioid would do. Buprenorphine is partial, meaning it only partially fills the receptor site. And then there's a third medication that we are, we use often is called naltrexone. Sometimes you might have heard of that like a Vivitrol shot or so this one can be provided also intramuscularly or taken as a pill every day as well. But what naltrexone does is it actually just completely blocks off this receptor site altogether. So this completely prevents any of the opioids to bind into this receptor at all. So when we're talking about reducing cravings, methadone and buprenorphine really do help with reducing cravings because it does help to stimulate that dopamine reward system a little bit. Whereas naltrexone really does not at all. So if somebody is really struggling with cravings, naltrexone is not necessarily the first line of medication to choose for that. So those are the three most commonly prescribed medications that are used for opioid use disorder treatment. And so each of these medications when kind of used as a part of more of a comprehensive treatment plan addresses different aspects of opioid dependence and supporting people through withdrawal and or their path to recovery. So again, we'll be going into that deeper on another session. All right, fentanyl. So fentanyl, its heightened potency compared to morphine or heroin is really attributed to its distinct chemical structure. So what this does is it creates a more tight bond to those opioid receptors in the brain and our spinal cord. So with a higher kind of attraction for these receptors, the rapid and a rapid set of onset, so it kicks in really quickly. Fentanyl produces the really powerful and immediate effect. So its chemical makeup makes for a quick distribution throughout the body. And it also and it also enhances that enhanced potency creates those really intense highs. But this also creates a really significant risk of overdose. And even just really, really small amounts of fentanyl can really have profound effects on our central nervous system and our respiratory system. And so this is kind of what makes it attractive on as an illicit drug on the street, because folks just need a little bit. But unfortunately, fentanyl is also the leading cause of overdose deaths right now. Its potency is estimated to be up to 100 times stronger than morphine. And, yeah, it's just the chemical structure makes it really, really challenging. And it also is harder to detect in routine drug screens. And so it makes it really hard to detect. And also, it's something that's really commonly found now in counterfeit drugs. In counterfeit pills. So a lot of times that is being added into these counterfeit pills. And so people are thinking they're taking something pharmaceutical, but really it's I've got another picture here I'll show you in a minute, but it makes it really dangerous because we don't really know how much fentanyl is in any of these things that people might be taking out on the street. Additionally, what makes it challenging is because of how it binds to our opioid receptors, it makes the things that we use to reverse overdoses not work as well. So like naloxone, for example, is what we use to reverse overdoses and opioid overdoses. And oftentimes it's not as easy to kick off the fentanyl that is bound to that receptor site as it is to, for example, as heroin. So in this photo, sorry, it's a little grainy, but as you can see, this is the amount of fentanyl that it takes for somebody to overdose versus the amount of heroin. So like I said, it's about 50 to a hundred times more potent than morphine and 50 times more potent than heroin. So fentanyl does have a place in our medical system in regard to when we're having surgical procedures done and it's highly monitored and dosed out properly and we are monitored and it makes it a really, really important medication for the medical system. However, on the street, it just really contributes to significant risks. And when it comes to the production of counterfeit pills, as I mentioned earlier, this is where it's actually quite dangerous because so in any medication, if it's produced in a lab, every medication has the active substance and some fillers and other matrix things that make up the rest of the pill essentially. And when it comes to making counterfeit pills, people don't have the means to make sure that every pill has the exact amount of medication or substance, active substance that they want to have in each pill. So oftentimes, you know, if you see this example down here, we'll have these, somebody will be mixing these substances together and creating tablets and pressing them. And unfortunately this pill, somebody might get and have no effects because there's no, let's call this fentanyl in there versus somebody who gets this pill and they have enough to overdose. Seven out of the 10 pills tested by the DEA have a potentially low dose of fentanyl. And these are just other examples of counterfeit drug seizures over the course of time. This is methamphetamine pills that are sold as MDMA or ecstasy, but it is not what they're thinking because they are actually getting methamphetamine. Again, these are also counterfeit methamphetamine pills. Then this is like an example real oxycodone versus a counterfeit. So if you don't know what you're really looking for, you might not know that this is not real. And same with Xanax, which is a benzodiazepine. But the second is also laced with a lot of fentanyl and cocaine. So this is naloxone. I'm not going to give an entire training right now on naloxone. Hopefully some of you have had training on naloxone, but naloxone is the medication that's used to help reverse opioid overdoses. So sometimes you probably have heard this called Narcan. Naloxone is just the actual medication name. Narcan is the brand name. But what this does is it helps to displace those opioids off of those receptor sites in our brain, which when that happens, kind of reverses the impact that the opioids have in our brains and our bodies. So that will restore our bodies kind of to go back to functioning normally. So by removing the opioids that are causing our breathing to slow, suddenly we're able to start breathing again. And same with our decrease in our heart rate, it'll just suddenly bring our heart rate back up. However, it's good to know that this is only a temporary fix. So it's really important that if you do end up using naloxone on somebody that it'll only usually work for a few minutes before, if they've had a lot, or especially if they are overdosing on fentanyl, it can potentially only last a few minutes and then they go back into overdose as the naloxone exits our system much faster than the opioids do. So it's very short acting. So it's really important to have extra doses of Narcan or naloxone, as well as call 9-1-1 and get actual emergency folks out to help with that. But again, here's just that example. Here's the opioid. We've got this bound to this receptor site and then in comes naloxone. Naloxone has the ability to just go and kick these opioids off the receptor site. And it kind of creates that short-term bond, allowing the person to kind of regain consciousness and come back until the opioids come back and move into the place of where the naloxone is. So, okay. All right. Okay. So that was kind of a really, really rapid, fast overview of brain science of substance use disorder and opioid use disorder. Again, next week, we're going to really dive deeper into those risk and prevention factors of what kind of causes people to have substance use disorder, as well as how can we do something to help prevent, what can we be doing to help prevent people from developing substance use disorders? And ultimately, all of this is really going to help us learn more about why different treatments work for opioid and substance use disorders. So, I'd love to open this time up for any questions or comments people might have about anything that we covered today. So, and I do have, I'm going to share this survey for folks to provide input on the session today as well. But I am going to quit talking and allow anybody who has any questions to come off mute or type in the chat any questions you might have. All right, and if there is no questions or comments today, then I think we can, we can wrap up and I think we're together again in the next week or two. And so if anytime you have questions that come up along the way. You're welcome to reach out or ask at our next session as well. So, all right. Thank you so much, Stephanie, and thank you all for joining us today, we will have our next session it looks like next Tuesday, the 13th so we'll hope to see you all then.

Opioid Response Network

tribal opioid response

native communities

substance use disorder

brain science

opioid receptors

medications for treatment

naloxone

fentanyl overdose